Morphine-induced antinociception

The existence of further alternative transcripts of MOP was postulated by the observation that in knockout mice with disrupted exon 1, heroin but not morphine was still analgesically active. Based on earlier observations that the antagonist naloxazone blocked morphine-induced antinociception but not morphine-induced respiratory depression, a subdivision of the MOP in pi and p2 was proposed. However, no discrete mRNA for each of these MOP subtypes has been found. It is, however, possible that subtypes of MOPs result from heterodimerization with other opioid receptors or by interaction with other proteins. 

Kang, Y.-M., Zhang, Z.-H., Yang, S.-W., Qiao, J.-T., Dafny, N. ATP-sensitive 1C channels are involved in the mediation of intrathecal norepinephrine- or morphine-induced antinociception at the spinal level a study using EMG planimetry of flexor reflex in rats, Brain Research Bulletin 1998a, 45, 269-273. 

In contrast, a low dose of the Ca2+ channel agonist BAY K 8644, a dihydropyridine derivative, antagonizes the antinociceptive effect of p-opioids. This is in agreement with results from Smith and Stevens (1995), who reported that Ca2+, when administered i.c.v., antagonizes morphine-induced antinociception in the mouse tail flick assay. The dose - response curve of morphine is shifted to the right by i.c.v. administration of calcium ions. 

Advokat, C. and Rhein, F. Q. Potentiation of morphine-induced antinociception in acute spinal rats by the NMDA antagonist dextrorphan, Brain Res. 1995, 699, 157-160. 

Hammond, D. L. Proudfit, H. K. (1980). Effects of locus coeruleus lesions on morphine-induced antinociception. Brain Res., 188, 79-91. 

Schmauss, C., and Herz, A. (1987). Intrathecally administered dynorphin-(l—17) modulates morphine-induced antinociception differently in morphine-naive and morphine-tolerant rats. Ewr. J. Pharmacol. 135, 429—431. 

Knockout mice with MOR-1 display profound gene dose-dependent reductions in the morphine-induced antinociception [73 75]. The availability... 

Chlornaltrexamine (/f-CNA, 15) another naltrexone derivative modified at C-6, is a nonequilibrium antagonist which blocks irreversibly the three major opioid receptor types (ji, k and 8). Portoghese and his collaborators have developed this compound as the first affinity labelling agent of its class [58-61]. Compound (15) has an alkylating function at C-6 (classic nitrogen mustards) able to bind covalently to opioid receptors. In the tail flick assay in mice, /f-CNA inhibited morphine-induced antinociception for 3-6... 

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